INTRODUCTION
Stroke is “a quickly evolving clinical symptoms of selective or widespread impairment of cognitive function that continues for more than 24 h” according to the World Health Organization (WHO).[ 1 ] A stroke happens when part of the brain does not have enough blood supply or interrupted, decreased oxygenation and nutrition’s to brain tissue. This disrupts the brain tissue by depriving it of oxygen and nutrients.[ 2 ]
According to a WHO estimate, 15 million people experience stroke annually, of which 33% (5 million) result in death and 33% in permanent disability. More seriously, a stroke episode occurs every split second, and a stroke-related death occurs every 10 s. In Saudi Arabia, stroke is the second contributor to mortality.[ 3 ] Its prevalence has been estimated to be 57.6% per each 100,000.[ 4 ]
Poststroke depression (PSD) is a typical neuropsychiatric symptom of high clinical significance since it has a detrimental effect on patients’ life quality and healing, obstructs rehabilitation, and places a significant burden on care providers. In addition, around 30% of stroke survivors have PSD, making it the most prevalent mental health condition.[ 5 ] PSD’s complex etiology is still completely understood. Although the majority of the research have not considered the length of the depression into account, a substantial number of significant studies have shown that PSD incidence is highest in the 1st year after a stroke occurrence and decreases thereafter.[ 6 ]
Several studies that examined the prevalence of PSD and its risk factors found that the following were substantially connected with PSD: cognitive impairment, stroke severity,[ 7 ] female gender,[ 7 ] and history of depression before the stroke.[ 8 ] Traumatic experiences in the month before the stroke begins,[ 9 ] a history of mental disorder, and smoking may also increase the risk of PSD in addition to the previously mentioned factors.[ 10 ] Furthermore, some researchers believe the location where the stroke occurred is a risk factor for developing PSD,[ 11 ] notwithstanding the findings of these investigations are conflicting and inconclusive.[ 12 ] For instance, Bhogal et al . found that patients with left hemisphere lesions had higher rates of depression.[ 13 ] While Wei’s systematic review found a significant correlation between the right hemisphere and PSD.[ 14 ]
Multiple factors that are crucial to management must be included and taken into consideration when determining and screening PSD. The current study aimed to estimate the prevalence of PSD and to determine the associated risk factors.
MATERIALS AND METHODS
Study population and setting
The adult patients currently being treated at King Saud University Medical City (n = 119) were studied using both primary and secondary data. The primary data were gathered by interviewing the patient at the neurology clinic and asking them about any symptoms of depression they were experiencing, while the secondary data were gathered by a review of the patient’s medical records.
This study includes all patients of both genders over the age of 18 years who had clinical stroke and were treated at the Neurology Department of the King Saud University Medical City-Riyadh, Saudi Arabia.
Previous strokes, speech difficulties with serious comprehension problems, a significant depression history before the stroke, and the existence of other chronic debilitating conditions (i.e., liver failure, renal failure, cancer, severe Parkinson’s disease, polyneuropathy, a history of psychiatric disease before the stroke, and severe cardiac diseases) were all considered exclusion criteria for this study.
Study tool and variables
The study tool was adapted from the items assessed in previous international studies exploring PSD. The main variables includes as follows:
Stroke
This study used a combination of clinical assessment, personal history, and neuroradiological results to make the stroke diagnosis (i.e., either a computed tomography scan, a magnetic resonance imaging, or both were performed on every subject).
Mood evaluation
Mood disorders were assessed on admission and 3–6 months after a stroke. Both individuals who scored 17 or higher on the Beck Depression Inventory (BDI)[ 15 ] and those who demonstrated clinically significant and ongoing depressive symptoms during their hospitalization or clinic visit were regarded as having depression.
Only neurologists evaluated all of the patients, and a psychiatrist subsequently had seen and monitored those with severe depression.
Demographic and risk factors
Information about patients age, gender, marital status, education level, profession, income, family history of psychiatric disorder as well as family history of chronic diseases were collected. Furthermore, data about patients’ history of comorbid diseases, psychiatric illness, and medications history were additionally added
Data collection
Data were collected through face-to-face interview conducted by the neurology residents and the trained data collectors. The obtained data were stored in a protected electronic format using an anonymous self-administered Google online questionnaire format.
Ethical considerations
The procedures followed in this study were in accordance with the ethical standards of the “KSU College of Medicine Research Center Institutional Review Board” IRB; project no. E-19-4076; and approval date: July 14, 2019). Participants were verbally consented to participate after being informed about the study. Participation was voluntary, and data were collected anonymously. All data were handled with strict confidentiality
Statistical analysis
The patients’ postdepression has been assessed using BDI Second Edition (BDI-II). BDI-II scores range between 0 and 63, with severity depression ratings of “minimal” (0–13), “mild” (14–19), “moderate” (20–28), and “severe” (29–63).[ 15 ] A cutoff of ≤17 was employed based on the BDI-II manual.[ 15 ]
Descriptive statistics were presented using numbers and percentages for all categorical variables while mean and standard deviation were used to present for all continuous variables. The relationship between the level of depression and the socio-demographic characteristics of the patients had been conducted using the Chi-square test or Fischer’s exact test (for values < 5). Based on significant results, a subsequent multivariate regression analysis had been performed to determine the independent significant factors of depression where the odds ratio and as well as 95% confidence interval (CI) were also reported. In addition, the comparison of the severity of depression according to stroke location and associated comorbidities has been performed using the Chi-square test and Fischer’s exact test (for values <5). A P = 0.05 was considered statistically significant. All statistical analyses were carried out using the Statistical Packages for Software Sciences (SPSS) version 26 Armonk, New York, USA, IBM Corporation.
RESULTS
This study involved 119 patients who suffered a stroke (56.3% females vs. 43.7% males). As shown in Table 1 , the most common age group was <60 years old (51.3%) with the majority being married (73.9%). With regards to education, 28.6% were high school graduates and 25.2% were bachelor’s degrees. With respect to monthly income, 26.1% were earning more than 3,000–5,000 SAR per month and another 26.1% were earning <1000 SAR per month. A family history of chronic diseases was reported by 92.4% of the patients while a family history of a psychiatric disorder has been reported by 53.8%. The most common stroke type was ischemic stroke (70.5%). The proportion of patients who use antidepressants after stroke was 28.6%.
Table 1: Sociodemographic characteristics of the patients (n =119)
Figure 1 depicts the associated comorbidities of the patients. It can be observed that the most associated comorbidities were diabetes (37%), hypertension (35.3%), and blood-related diseases (15.1%).
Figure 1: Associated comorbidities
Regarding PSD [Table 2 ], the prevalence of clinically depressed patients was 76.5% while 23.5% were not clinically depressed. Regarding the severity of depression, minimal, mild, moderate, and severe depression were detected among 13.4%, 27.7%, 38.7%, and 20.2%, respectively [Figure 2 ].
Table 2: Prevalence of clinically significant depression according to the Beck Depression Inventory Questionnaire (n =119)
Figure 2: Severity of depression
When measuring the relationship between the level of depression and the socio-demographic characteristics of the patients, it was observed that the prevalence of depression was significantly more common among gender females (P = 0.003), unemployed (P = 0.016), patients with less monthly income (P = 0.013) and those with a family history of psychiatric disorder (P = 0.011) while age group, marital status, educational level, use of anti-depressants, and associated comorbidities did not show a significant relationship with the level of depression (P > 0.05) [Table 3 ].
Table 3: Relationship between the level of depression and the sociodemographic characteristics of the patients (n =119)
When conducting a multivariate regression model, it was found that only the family history of psychiatric disorder remained significant and determined as the only independent significant factor of depression. This further indicates that patients who were unsure of a family history of a psychiatric disorder were predicted to increase the risk of having depression by 7.051-fold higher than those who have known about it (Adjusted odd ratio [AOR] = 7.051; 95% CI = 1.35136.804; P = 0.021). Other variables included in the model did not significant effect on depression including gender, profession, and monthly income (P > 0.05) [Table 4 ].
Table 4: Multivariate regression analysis to determine the effect of depression among the selected sociodemographic characteristics of the patients (n =119)
As shown in Table 5 , no significant differences were observed between the severity of depression according to stroke location (P = 0.166), diabetes (P = 0.245), hypertension (P = 0.172), and obesity (P = 0.184). However, significant differences were observed between the severity of depression and multiple comorbidities (P = 0.001).
Table 5: Severity of depression according to stroke location and comorbidities (n =119)
DISCUSSION
The Diagnostic and Statistical Manual, Fifth Edition defines poststroke mood disorders as mood disorders with depressive symptoms, major depressive episode, or mixed-mood characteristics.[ 16 ] A patient with a major depression-like episode spurred on by a stroke must exhibit four other symptoms of depression for at least 2 weeks in addition to a depressed mood or loss of interest or pleasure. Recognizing and treating PSD is crucial for better rehabilitation results.[ 17–19 ] Current stroke recommendations also advocate for the early detection and treatment of depression.[ 20 ]
PSD rates in the preponderance of the study range from 20% to 79%, and may surpass 84%, based on the demographics examined.[ 18 , 21 , 22 ] In the present study, PSD was present in 76.5% of subjects. Moreover, it was shown that 38.7% and 20.2% of individuals, respectively, had moderate and severe depression, while 27.7% of people had mild depression. In comparison to the percentage from Saudi Arabia and other Arab nations that had previously been reported, our results were much higher.[ 22–24 ] More than two-thirds of the participants were younger than 65, which has been identified in prior studies as a risk factor for PSD and may account for these high percentages.[ 25 , 26 ] In addition, because these data were collected during the second wave of corona (delta variant), it could reflect the effects of depression and anxiety associated with the COVID-19 pandemic.[ 27 , 28 ]
Demographic variables are important determination of PSD. Similar results were seen in our study, where it was shown that female (P = 0.003), patients without jobs (P = 0.016), and patients with low incomes (P = 0.013) were much more likely to experience depression. This result agrees with the vast majority of earlier studies.[ 29–32 ] Numerous studies show that women are at higher risk than men for developing PSD.[ 29 , 30 ] Given that depression is more common in women than men overall, with odds ratios ranging from 1.33 to 2.40 across numerous studies, it is possible that this association between female gender and PSD is caused by a number of factors, including the incidence of depression in the general population.[ 33 , 34 ] Due to its effects on the moods of female patients, hormonal changes have been the subject of some additional research, which may have contributed to this conclusion.[ 35 ] Another explanation could be social variables, such as gender-specific exposure to stressors.[ 34 ]
On the other hand, we found no evidence of a significant relationship between PSD and age, marital status, or educational attainment. Age as a risk factor for PSD has inconsistent evidence to support it. Age <70 years was cited as a risk factor for PSD in a number of earlier studies.[ 25 , 26 , 36 ] However, elderly people are more susceptible to PSD, according to different studies.[ 37 , 38 ] In addition, several studies have found no relationship between age and the occurrence of PSD.[ 18 ] Our results contradict with those of other researchers, such Zan Wang et al . and Astrom, who have concluded that widowhood, divorce, and living solitary are all associated with depression.[ 39 , 40 ]
Our study strongly supports a substantial relationship (P = 0.011) between PSD and a family history of mental illness. Furthermore, according to the most recent data, having a family history of mental illnesses increases the probability of developing PSD by 7.051 times (AOR = 7.051; 95% CI = 49.085; P = 0.011). This result is consistent with a number of earlier research.[ 41 , 42 ] The genetic history that gives susceptibility and resiliency to the development of mental illnesses when an individual encounters an unanticipated stressful environment is one of the potential causes of this finding. Some possible genes, such as 5-HTTLPR, the STin2 VNTR polymorphisms of the serotonin transporter gene, and increased brain-derived neurotrophic factor, have been identified as PSD risk factors.[ 40 , 42–45 ] Several studies revealed that PSD is more closely associated with the location and intensity of the stroke than the presence of a positive family history of a mental condition. They also connected PSD to infarcts in the left frontal or basal ganglia.[ 46 ] In fact, they suggested that patient with no history of mental illness in their families could still be at risk for developing PSD after having a major stroke, particularly on the left side of the brain.
In the present studies, it was not discovered that vascular risk factors such diabetes, hypertension smoking, hyperlipidemia, and obesity were independent predictors of PSD. Despite the fact that 64 patients (53.7%) had at least one concomitant medical condition before the stroke. Hypertension (35.3%) and diabetes mellitus (37.4%) were the two most common stroke risk factors. Our findings are consistent with those of earlier studies.[ 19 , 31 , 47 ]
Approximately 84 patients, or 70.5% of the study’s participants, experienced ischemic strokes, which are the most common type of stroke lesion. Alternatively, 20 patients (16.8%) experienced hemorrhagic strokes, which comprised intracerebral and subarachnoid hemorrhages. PSD was experienced by 11 of the 15 people (12.6%) who had transient ischemic episodes. No correlation between PSD and the type of stroke or the affected side of the brain was discovered by our study. Recent systematic reviews validate our findings and refute any link between PSD and stroke cause (ischemic or hemorrhagic stroke) or stroke type (thrombotic and embolic).[ 19 , 31 , 47 ] Unfortunately, the precise location of the strokes or the degree of brain tissue destruction was not recorded in this study. These factors are crucial for determining if someone would develop PSD, as studies have shown that higher neurological tissue loss increases the likelihood of PSD.[ 48 ] Recent research has emphasized the importance of stroke site in the formation of the PSD. In particular, they suggested that frontal lobe/anterior strokes are linked to increased incidence of PSD compared to strokes in other areas.[ 17 ]
Despite their PSD symptoms, a considerable number of patients (71.4%) did not consult a psychiatrist or take antidepressant medication. This is cause for concern in this study and may have an impact on how severe their PSD is over the course of ongoing follow-up. No statistically significant correlation between the usage of antidepressants and PSD was discovered in the present study. However, prior research with substantial sample sizes highlighted the significance of early antidepressant medication initiation in the prevention of PSD development.[ 49–51 ] According to a new study that supports previous findings, patients with PSD who responded to nortriptyline or fluoxetine treatment showed noticeably superior improvement in their daily routines than those who did not respond to active treatment or control.[ 52 ] As a result, we must regularly test both acute and chronic stroke survivors for depression and implement the necessary interventions.
This study’s limitations include the exclusion of individuals with more severe strokes who were unable to properly converse due to aphasia. Other significant factors, such as the location of the stroke, the degree of cognitive dysfunctions, the level of social support, and the intensity of the stroke were not taken into account. However, these factors could influence the prevalence of PSD in stroke patients.
CONCLUSION
In this study, two-thirds of the stroke survivors experience PSD. It is mostly correlated with sociodemographic factors such female gender, mental illness in the family history, unemployment, and low income. Likewise, PSD may also be predicted by a family history of mental illness.
Patients consent
Consent was obtained from all patients.
Ethical approval
Ethical approval for the research was obtained from the Ethics Review Committee at King Saud University Medical City in Riyadh #E-19-4076.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
REFERENCES
1. Coupland AP, Thapar A, Qureshi MI, Jenkins H, Davies AH. The definition of stroke. J R Soc Med 2017;110:9–12.
2. Al-Harbi N, Alrasheedi MS, Alshammari ST. Hemoglobin level is associated with severe stroke among stroke patients in Saudi Arabia. Int J Health Sci (Qassim) 2020;14:18–22.
3. Al-Senani F, Al-Johani M, Salawati M, Alhazzani A, Morgenstern LB, Seguel Ravest V, et al. An epidemiological model for first stroke in Saudi Arabia. J Stroke Cerebrovasc Dis 2020;29:104465.
4. Alhazzani AA, Mahfouz AA, Abolyazid AY, Awadalla NJ, Aftab R, Faraheen A, et al. Study of stroke incidence in the Aseer Region, Southwestern Saudi Arabia. Int J Environ Res Public Health 2018;15:215.
5. Paolucci S, Iosa M, Coiro P, Venturiero V, Savo A, De Angelis D, et al. Post-stroke depression increases disability more than 15% in ischemic stroke survivors:A case-control study. Front Neurol 2019;10:926 doi:10.3389/fneur.2019.00926.
6. Das J, Rajanikant GK. Post stroke depression:The sequelae of cerebral stroke. Neurosci Biobehav Rev 2018;90:104–14.
7. Hackett ML, Anderson CS. Predictors of depression after stroke:A systematic review of observational studies. Stroke 2005;36:2296–301.
8. Ayerbe L, Ayis S, Crichton S, Wolfe CD, Rudd AG. The natural history of depression up to 15 years after stroke:The South London Stroke Register. Stroke 2013;44:1105–10.
9. Guiraud V, Gallarda T, Calvet D, Turc G, Oppenheim C, Rouillon F, et al. Depression predictors within six months of ischemic stroke:The DEPRESS study. Int J Stroke 2016;11:519–25.
10. Robinson RG, Starr LB, Kubos KL, Price TR. A two-year longitudinal study of post-stroke mood disorders:Findings during the initial evaluation. Stroke 1983;14:736–41.
11. de Man-van Ginkel JM, Hafsteinsdóttir TB, Lindeman E, Ettema RG, Grobbee DE, Schuurmans MJ. In-hospital risk prediction for post-stroke depression:Development and validation of the post-stroke depression prediction scale. Stroke 2013;44:2441–5.
12. Singh A, Herrmann N, Black SE. The importance of lesion location in poststroke depression:A critical review. Can J Psychiatry 1998;43:921–7.
13. Bhogal SK, Teasell R, Foley N, Speechley M. Lesion location and poststroke depression:Systematic review of the methodological limitations in the literature. Stroke 2004;35:794–802.
14. Wei N, Yong W, Li X, Zhou Y, Deng M, Zhu H, et al. Post-stroke depression and lesion location:A systematic review. J Neurol 2015;262:81–90.
15. Beck AT, Steer RA, Brown GK Manual for the Beck Depression Inventory-II 1 San Antonio, TX Psychological Corporation 1996 10–37.
16. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders –DSM-IV Washington, DC American Psychiatric Press 1994.
17. Robinson RG, Jorge RE. Post-stroke depression:A review. Am J Psychiatry 2016;173:221–31.
18. Hackett M, Pickles K. Part 1:Frequency of depression after stroke:An updated systematic review and meta-analysis of observational studies. World Stroke Organ 2014;9:1017–25.
19. Kutlubaev M, Hackett M. Part II:Predictors of depression after stroke and impact of depression on stroke outcome:An updated systematic review of observational studies. World Stroke Organ 2014;9:1026–36.
20. Winstein CJ, Stein J, Arena R, Bates B, Cherney LR, Cramer SC, et al. Guidelines for adult stroke rehabilitation and recovery:A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2016;47:e98–169.
21. Bar M, Skoloudik D, Roubec M. Post-stroke depression:A one year prospective follow-up study. J Neurol Sci 2009;285:S172.
22. Lökk J, Delbari A. Management of depression in elderly stroke patients. Neuropsychiatr Dis Treat 2010;6:539–49.
23. Al-Arjan S, Shirley T, Nadina L. Prevalence of post-stroke emotional disorders in Saudi Arabia. Phys Med Rehabil Int 2015;2:1033.
24. Kaadan MI, Larson MJ. Management of post-stroke depression in the Middle East and North Africa:Too little is known. J Neurol Sci 2017;378:220–4.
25. Carota A, Berney A, Aybek S, Iaria G, Staub F, Ghika-Schmid F, et al. Aprospective study of predictors of poststroke depression. Neurology 2005;64:428–33.
26. Li J, Zhao YD, Zeng JW, Chen XY, Wang RD, Cheng SY. Serum brain-derived neurotrophic factor levels in post-stroke depression. J Affect Disord 2014;168:373–9.
27. Wong LP, Alias H, Md Fuzi AA, Omar IS, Mohamad Nor A, Tan MP, et al. Escalating progression of mental health disorders during the COVID-19 pandemic:Evidence from a nationwide survey. PLoS One 2021;16:e0248916.
28. Santomaur D. Global prevalence and burden of depressive and anxiety disorders in 204 countries and territories in 2020 due to the COVID-19 pandemic. Lancet 2021;398:1700–12.
29. Medeiros GC, Roy D, Kontos N, Beach SR. Post-stroke depression:A 2020 updated review. Gen Hosp Psychiatry 2020;66:70–80.
30. Paolucci S, Gandolfo C, Provinciali L, Torta R, Toso V. DESTRO Study Group. The Italian multicenter observational study on post-stroke depression (DESTRO). J Neurol 2006;253:556–62.
31. De Ryck A, Brouns R, Geurden M, Elseviers M, De Deyn PP, Engelborghs S. Risk factors for poststroke depression:Identification of inconsistencies based on a systematic review. J Geriatr Psychiatry Neurol 2014;27:147–58.
32. Khedr EM, Abdelrahman AA, Desoky T, Zaki A, Gamea A. Post-stroke depression:Frequency, risk factors, and impact on quality of life among 103 stroke patients-hospital-based study. Egypt J Neurol Psychiatry Neurosurg 2020;56:66 https://doi.org/10.1186/s41983-020-00199-8.
33. Acciai F, Hardy M. Depression in later life:A closer look at the gender gap. Soc Sci Res 2017;68:163–75.
34. Hopcroft RL, McLaughlin J. Why is the sex gap in feelings of depression wider in high gender equity countries?The effect of children on the psychological well-being of men and women. Soc Sci Res 2012;41:501–13.
35. Beekman AT, Copeland JR, Prince MJ. Review of community prevalence of depression in later life. Br J Psychiatry 1999;174:307–11.
36. Shi Y, Yang D, Zeng Y, Wu W. Risk factors for post-stroke depression:A meta-analysis. Front Aging Neurosci 2017;9:218.
37. Cheng LS, Tu WJ, Shen Y, Zhang LJ, Ji K. Combination of high-sensitivity C-reactive protein and homocysteine predicts the post-stroke depression in patients with ischemic stroke. Mol Neurobiol 2018;55:2952–8.
38. Jørgensen TS, Wium-Andersen IK, Wium-Andersen MK, Jørgensen MB, Prescott E, Maartensson S, et al. Incidence of depression after stroke, and associated risk factors and mortality outcomes, in a large cohort of Danish patients. JAMA Psychiatry 2016;73:1032–40.
39. Aström M, Olsson T, Asplund K. Different linkage of depression to hypercortisolism early versus late after stroke. A 3-year longitudinal study. Stroke 1993;24:52–7.
40. Wang Z, Shi Y, Liu F, Jia N, Gao J, Pang X, et al. Diversiform etiologies for post-stroke depression. Front Psychiatry 2018;9:761.
41. Tenev VT, Robinson RG, Jorge RE. Is family history of depression a risk factor for poststroke depression?Meta-analysis. Am J Geriatr Psychiatry 2009;17:276–80.
42. Kohen R, Cain KC, Mitchell PH, Becker K, Buzaitis A, Millard SP, et al. Association of serotonin transporter gene polymorphisms with poststroke depression. Arch Gen Psychiatry 2008;65:1296–302.
43. Kim JM, Stewart R, Kang HJ, Kim SW, Shin IS, Kim HR, et al. Alongitudinal study of SLC6A4 DNA promoter methylation and poststroke depression. J Psychiatr Res 2013;47:1222–7.
44. Zhou Z, Ding X, Yang Q, Hu J, Shang X, Huang X, et al. Association between single-nucleotide polymorphisms of the tyrosine kinase receptor B (TrkB) and post-stroke depression in China. PLoS One 2015;10:e0144301.
45. Li XB, Wang J, Xu AD, Huang JM, Meng LQ, Huang RY, et al. Apolipoprotein E polymorphisms increase the risk of post-stroke depression. Neural Regen Res 2016;11:1790–6.
46. Starkstein SE, Robinson RG, Berthier ML, Parikh RM, Price TR. Differential mood changes following basal ganglia ERSU thalamic lesions. Arch Neurol 1988;45:725–30.
47. Johnson JL, Minarik PA, Nyström KV, Bautista C, Gorman MJ. Poststroke depression incidence and risk factors:An integrative literature review. J Neurosci Nurs 2006;38:316–27.
48. Nickel A, Thomalla G. Post-stroke depression:Impact of lesion location and methodological limitations-A topical review. Front Neurol 2017;8:498.
49. Zhang S, Xu M, Liu ZJ, Feng J, Ma Y. Neuropsychiatric issues after stroke:Clinical significance and therapeutic implications. World J Psychiatry 2020;10:125–38.
50. Salter KL, Foley NC, Zhu L, Jutai JW, Teasell RW. Prevention of poststroke depression:Does prophylactic pharmacotherapy work?. J Stroke Cerebrovasc Dis 2013;22:1243–51.
51. Cui M, Huang CY, Wang F. Efficacy and safety of citalopram for the treatment of poststroke depression:A meta-analysis. J Stroke Cerebrovasc Dis 2018;27:2905–18.
52. Chemerinski E, Robinson RG, Arndt S, Kosier JT. The effect of remission of poststroke depression on activities of daily living in a double-blind randomized treatment study. J Nerv Ment Dis 2001;189:421–5.
